In terms of animal research, there is a body of literature that has documented stretch-induced hypertrophy. Goldspink (18) compared 2 conditions where rat soleus and extensor digitorum longus muscles were immobilized in shortened and lengthened positions and reported that the lengthened muscles increased in size, whereas shortened position muscles atrophied. This suggests that passive stretch at long muscle length stimulates protein synthesis and induces the growth of muscles.
Holly et al. (27) reported increases in length and cross-sectional area of 4 chicken wing muscles stretched to different extents over a 5-week duration. Essentially, length changes were complete after 1 week of stretching; however, increases in cross-sectional area of 73-206% were recorded over the 5-week duration of the study depending on the type of the muscle. The researchers concluded that muscle grew and adapted enzymatically (oxidative enzymes) to stretch, but these responses are dissimilar in twitch and tonic muscles.
Goldspink et al. (19) investigated the effect of passive stretch, electrical stimulation at 10 Hz, and a combination of both stretch and electrical stimulation, on the expression of insulin-like growth factor I (IGF-I) and the rates of protein turnover and growth of the rabbit extensor digitorum longus muscle. It was found that static stretch caused significant adaptive growth and increases in IGF-I either with or without electrical stimulation, whereas continuous electrical stimulation alone failed to induce muscle growth. Yang et al. (67) studying rabbit's lower limb muscles found that 6 days of passive stretch while immobilized in a plaster cast not only induced an increase in expression of IGF-I messenger RNA (mRNA) but also increased the percentage of fibers expressing slow myosin. This change in muscle phenotype was accompanied by a rapid and marked increase in muscle mass, total RNA content, and IGF-I gene expression.
Unlike the previous studies that used chronic stretching protocols, a study by Coutinho et al. (12), which was conducted on eighteen 16-week-old Wistar rats for 3 weeks, found that stretching the immobilized soleus muscles for 40 minutes every 3 days did prevent the muscle shortening and reduced the magnitude of muscle atrophy as compared with a immobilized-only group (22 ± 40 versus 37 ± 31%, respectively). Furthermore, muscles that were submitted to a stretching-only group significantly increased the length (5 ± 2%), serial sarcomere number (4 ± 4%), and fiber area (16 ± 44%) compared with the contralateral muscles. This study showed that although the stretching was passive, hypertrophy still resulted. Tension is also an important regulator of skeletal muscle hypertrophy in vivo because when increased constant tension is applied to embryonic skeletal muscle fibers differentiated in a tissue culture environment, many of the same biochemical processes associated with muscle hypertrophy in vivo are also stimulated in vitro, for example, protein synthesis, total protein, and myosin heavy-chain accumulation (62).
Although much of the research in this area is from immobilization studies, it can be observed that active and passive stretch can induce changes in cross-sectional area of the muscle (14). Naturally, a muscle is stretched under load during strength training, and the slow tempos recommended for hypertrophic adaptation magnify the time under tension or stretch load. During the rest periods, if the muscles are actively or passively stretched, the additional mechanical stimulus may enhance the hypertrophic effect. This contention obviously needs to be researched in a systematic manner, ensuring that the stretching protocol does not significantly influence the ensuing repetition and set kinematics and kinetics.